Morphine increases striatal dopamine turnover rate. This increase is probably due to stimulation of opiate receptors located on DA nerve terminals of striatum. Morphine injected in substantia nigra (SN) failed to change striatal DA metabolism but blocked the activation of TH by haloperidol. This action of morphine was not reversed by bicuculline. Since opiate receptors in SN are located on neurons connecting the SN with the forebrain (possibly on substance P neurons), these results suggest that intranigral morphine prevents the haloperidol-induced activation of striatal TH by interfering with a non-GABAergic (perhaps substance P) projection to SN. The role of opiate receptors located on catecholaminergic cells was studied using primary culture of adrenal chromaffin cells. These cells have measurable amounts of opiate receptors. Stimuation of these receptors with agonists decreases the relase of catecholamine elicited by nicotine. The results suggest that stimulation of opiate receptors modulates allosterically the function of nicotinic and perhaps other receptors located on the chromaffin cell membranes.